Astroglial Heme Oxygenase-1 and the Origin of Corpora Amylacea in Aging and Degenerating Neural Tissues
Identifieur interne : 000B39 ( Main/Exploration ); précédent : 000B38; suivant : 000B40Astroglial Heme Oxygenase-1 and the Origin of Corpora Amylacea in Aging and Degenerating Neural Tissues
Auteurs : Wei Song [Canada] ; Hillel Zukor [Canada] ; Adrienne Liberman [Canada] ; Sagi Kaduri [Canada] ; Zoe Arvanitakis [États-Unis] ; David A. Bennett [États-Unis] ; Hyman M. Schipper [Canada]Source :
- Experimental neurology [ 0014-4886 ] ; 2014.
Abstract
Corpora amylacea (CA) are glycoproteinaceous (predominantly glial and extracellular) inclusions that accumulate in normal aging brain and, to a greater extent, in Alzheimer disease (AD). Previous pharmacological evidence suggested that up-regulation of endogenous heme oxygenase-1 (HO-1) in astrocytes promotes transformation of normal mitochondria to CA-like inclusions. Here, we determined whether 1)
CA were ascertained in (i) neonatal rat astroglia transfected with flag-tagged human HO-1 cDNA, (ii) brain sections derived from 19 month-old GFAP.HMOX1 and wild-type (WT) mice, and (iii) post-mortem hippocampal sections from individuals with mild (MCI) and no cognitive impairment (NCI) after staining with PAS or antisera against HO-1, ubiquitin (Ub), manganese suoperoxide dismutase (MnSOD), α-synuclein or tyrosine hydroxylase (TH).
HO-1 promotes mitochondrial damage and CA biogenesis in astrocyte cultures and in the intact aging brain. CA formation is enhanced in the MCI hippocampus and thus occurs relatively early in the pathogenesis of AD. Glial HO-1 suppression may attenuate bioenergetic failure and slow disease progression in AD and other neurodegenerative conditions featuring accelerated accumulation of CA.
Url:
DOI: 10.1016/j.expneurol.2014.01.006
PubMed: 24440642
PubMed Central: 4020524
Affiliations:
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Catherine Road, Montreal, Quebec H3T 1E2, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Lady Davis Institute, Jewish General Hospital, 3755 Cote Ste. Catherine Road, Montreal, Quebec H3T 1E2</wicri:regionArea><wicri:noRegion>Quebec H3T 1E2</wicri:noRegion></affiliation></author><author><name sortKey="Zukor, Hillel" sort="Zukor, Hillel" uniqKey="Zukor H" first="Hillel" last="Zukor">Hillel Zukor</name><affiliation wicri:level="1"><nlm:aff id="A1">Lady Davis Institute, Jewish General Hospital, 3755 Cote Ste. Catherine Road, Montreal, Quebec H3T 1E2, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Lady Davis Institute, Jewish General Hospital, 3755 Cote Ste. Catherine Road, Montreal, Quebec H3T 1E2</wicri:regionArea><wicri:noRegion>Quebec H3T 1E2</wicri:noRegion></affiliation><affiliation wicri:level="4"><nlm:aff id="A2">Dept. of Neurology and Neurosurgery, McGill University, Montreal, Quebec H3A 2B4, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Dept. of Neurology and Neurosurgery, McGill University, Montreal, Quebec H3A 2B4</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author><author><name sortKey="Liberman, Adrienne" sort="Liberman, Adrienne" uniqKey="Liberman A" first="Adrienne" last="Liberman">Adrienne Liberman</name><affiliation wicri:level="1"><nlm:aff id="A1">Lady Davis Institute, Jewish General Hospital, 3755 Cote Ste. Catherine Road, Montreal, Quebec H3T 1E2, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Lady Davis Institute, Jewish General Hospital, 3755 Cote Ste. Catherine Road, Montreal, Quebec H3T 1E2</wicri:regionArea><wicri:noRegion>Quebec H3T 1E2</wicri:noRegion></affiliation></author><author><name sortKey="Kaduri, Sagi" sort="Kaduri, Sagi" uniqKey="Kaduri S" first="Sagi" last="Kaduri">Sagi Kaduri</name><affiliation wicri:level="1"><nlm:aff id="A1">Lady Davis Institute, Jewish General Hospital, 3755 Cote Ste. Catherine Road, Montreal, Quebec H3T 1E2, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Lady Davis Institute, Jewish General Hospital, 3755 Cote Ste. Catherine Road, Montreal, Quebec H3T 1E2</wicri:regionArea><wicri:noRegion>Quebec H3T 1E2</wicri:noRegion></affiliation></author><author><name sortKey="Arvanitakis, Zoe" sort="Arvanitakis, Zoe" uniqKey="Arvanitakis Z" first="Zoe" last="Arvanitakis">Zoe Arvanitakis</name><affiliation wicri:level="1"><nlm:aff id="A3">Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, Illinois 60612, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, Illinois 60612</wicri:regionArea><wicri:noRegion>Illinois 60612</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="A4">Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612</wicri:regionArea><wicri:noRegion>Illinois 60612</wicri:noRegion></affiliation></author><author><name sortKey="Bennett, David A" sort="Bennett, David A" uniqKey="Bennett D" first="David A." last="Bennett">David A. Bennett</name><affiliation wicri:level="1"><nlm:aff id="A3">Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, Illinois 60612, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, Illinois 60612</wicri:regionArea><wicri:noRegion>Illinois 60612</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="A4">Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612</wicri:regionArea><wicri:noRegion>Illinois 60612</wicri:noRegion></affiliation></author><author><name sortKey="Schipper, Hyman M" sort="Schipper, Hyman M" uniqKey="Schipper H" first="Hyman M." last="Schipper">Hyman M. Schipper</name><affiliation wicri:level="1"><nlm:aff id="A1">Lady Davis Institute, Jewish General Hospital, 3755 Cote Ste. Catherine Road, Montreal, Quebec H3T 1E2, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Lady Davis Institute, Jewish General Hospital, 3755 Cote Ste. Catherine Road, Montreal, Quebec H3T 1E2</wicri:regionArea><wicri:noRegion>Quebec H3T 1E2</wicri:noRegion></affiliation><affiliation wicri:level="4"><nlm:aff id="A2">Dept. of Neurology and Neurosurgery, McGill University, Montreal, Quebec H3A 2B4, Canada</nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Dept. of Neurology and Neurosurgery, McGill University, Montreal, Quebec H3A 2B4</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author></analytic><series><title level="j">Experimental neurology</title><idno type="ISSN">0014-4886</idno><idno type="eISSN">1090-2430</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title><p id="P2">Corpora amylacea (CA) are glycoproteinaceous (predominantly glial and extracellular) inclusions that accumulate in normal aging brain and, to a greater extent, in Alzheimer disease (AD). Previous pharmacological evidence suggested that up-regulation of endogenous heme oxygenase-1 (HO-1) in astrocytes promotes transformation of normal mitochondria to CA-like inclusions. Here, we determined whether 1) <italic>HMOX1</italic> transfection fosters the accumulation of CA-like inclusions in cultured rat astroglia; 2) the <italic>HMOX1</italic> transgene promotes CA formation in the brains of aging GFAP.HMOX1 mice; and 3) brain mitochondrial damage and CA biogenesis are augmented in persons with mild cognitive impairment (MCI), a harbinger of AD.</p></sec><sec id="S2"><title>Methods</title><p id="P3">CA were ascertained in (i) neonatal rat astroglia transfected with flag-tagged human HO-1 cDNA, (ii) brain sections derived from 19 month-old GFAP.HMOX1 and wild-type (WT) mice, and (iii) post-mortem hippocampal sections from individuals with mild (MCI) and no cognitive impairment (NCI) after staining with PAS or antisera against HO-1, ubiquitin (Ub), manganese suoperoxide dismutase (MnSOD), α-synuclein or tyrosine hydroxylase (TH).</p></sec><sec id="S3"><title>Results</title><p id="P4"><italic>HMOX1</italic> transfection induced cytoplasmic vacuolation and the accumulation of PAS+ inclusions in cultured astroglia. Numerous CA-like inclusions stained with PAS− and immunoreactive for HO-1, Ub and MnSOD were observed in the brains of GFAP.HMOX1 mice, but were rarely encountered in age-matched, wild-type controls. Numbers of HO-1-positive CA were significantly increased in certain hippocampal strata of MCI subjects relative to NCI preparations. MnSOD and Ub proteins co-localized to CA in both the control and MCI specimens.</p></sec><sec id="S4"><title>Conclusions</title><p id="P5">HO-1 promotes mitochondrial damage and CA biogenesis in astrocyte cultures and in the intact aging brain. CA formation is enhanced in the MCI hippocampus and thus occurs relatively early in the pathogenesis of AD. Glial HO-1 suppression may attenuate bioenergetic failure and slow disease progression in AD and other neurodegenerative conditions featuring accelerated accumulation of CA.</p></sec></div></front></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country><region><li>Québec</li></region><settlement><li>Montréal</li></settlement><orgName><li>Université McGill</li></orgName></list><tree><country name="Canada"><noRegion><name sortKey="Song, Wei" sort="Song, Wei" uniqKey="Song W" first="Wei" last="Song">Wei Song</name></noRegion><name sortKey="Kaduri, Sagi" sort="Kaduri, Sagi" uniqKey="Kaduri S" first="Sagi" last="Kaduri">Sagi Kaduri</name><name sortKey="Liberman, Adrienne" sort="Liberman, Adrienne" uniqKey="Liberman A" first="Adrienne" last="Liberman">Adrienne Liberman</name><name sortKey="Schipper, Hyman M" sort="Schipper, Hyman M" uniqKey="Schipper H" first="Hyman M." last="Schipper">Hyman M. Schipper</name><name sortKey="Schipper, Hyman M" sort="Schipper, Hyman M" uniqKey="Schipper H" first="Hyman M." last="Schipper">Hyman M. Schipper</name><name sortKey="Zukor, Hillel" sort="Zukor, Hillel" uniqKey="Zukor H" first="Hillel" last="Zukor">Hillel Zukor</name><name sortKey="Zukor, Hillel" sort="Zukor, Hillel" uniqKey="Zukor H" first="Hillel" last="Zukor">Hillel Zukor</name></country><country name="États-Unis"><noRegion><name sortKey="Arvanitakis, Zoe" sort="Arvanitakis, Zoe" uniqKey="Arvanitakis Z" first="Zoe" last="Arvanitakis">Zoe Arvanitakis</name></noRegion><name sortKey="Arvanitakis, Zoe" sort="Arvanitakis, Zoe" uniqKey="Arvanitakis Z" first="Zoe" last="Arvanitakis">Zoe Arvanitakis</name><name sortKey="Bennett, David A" sort="Bennett, David A" uniqKey="Bennett D" first="David A." last="Bennett">David A. Bennett</name><name sortKey="Bennett, David A" sort="Bennett, David A" uniqKey="Bennett D" first="David A." last="Bennett">David A. 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